Histology of Kidney

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Kidney

DR. AYMEN SANA


PG1 MPHIL ANATOMY
Learning Objectives

 Describe the histological features of the


nephron
 Describe the histological features of renal
corpuscle s and filtration apparatus with
relation to clinical conditions
Urinary system

Water and electrolytes Homeostasis

Excretion of metabolic wastes

Excretion of many bioactive substances

Regulation of arterial blood pressure by


secretion of RENIN
Urinary system

Secretion of erythropoietin

Conversion of the steroid


prohormone vitamin D

Gluconeogenesis
KIDNEYS

Capsule

Hilum

Renal pelvis

Major calyces

Minor calyces
KIDNEYS

Outer cortex

Inner medulla

Renal pyramids

Renal columns.

Renal lobe

Medullary rays

Renal papilla
Capsule

The kidney surface is covered by a connective tissue capsule.

Outer layer of fibroblasts and collagen fibers

Inner layer with a cellular component of myofibroblasts

Capsule passes inward at the hilum, where it forms the connective


tissue covering of the sinus and becomes continuous with the
connective tissue forming the walls of the calyces and renal pelvis
Capsule of Kidney
Cortex

The outer reddish-


brown part

Characterized by renal
corpuscles and their
associated tubules
Medulla

The much lighter colored


inner part

Characterized by
straight tubules,
collecting ducts, and a
special capillary
network, the vasa recta
Nephron

Structural and
Functional
Unit of
Kidneys
Nephrons

Renal corpuscle

Proximal tubule

Loop of Henle

Distal tubule

Connecting tubule
Nephrons

Cortical nephrons

Juxtamedullary
nephrons (one
seventh)
Blood
circulation

Collectively, the
cortex receives
over 10 times
more blood than
the medulla.
Kidney with the renal artery
injected with carmine dye
before fixation.
Clinical Corelation

Polycystic kidney disease is an


inherited disorder in which normal
cortical organization of both
kidneys is lost due to the
formation of multiple, large, fluid-
filled cysts. The cysts may arise
from any epithelial cells of the
nephron and can lead to gross
kidney enlargement and loss of
renal function.
Clinical Corelation

Inflammation within the glomeruli,


or glomerulonephritis, which can
range from acute or chronic,
usually stems from humoral
immune reactions.
Clinical Corelation

Varieties of this condition involve the


deposition of circulating antibody-antigen
complexes within glomeruli or circulating
antibodies binding to either glomerular
antigens or extraneous antigens
deposited in the glomeruli. Immune
complexes can then elicit a local
inflammatory response.
Renal function

Filtration

Secretion

Reabsorption
Renal Corpuscles & Blood Filtration

Bowman capsule

Parietal layer
Capsular (or urinary)
space
Visceral layer

Podocytes
Visceral layer of
Bowman’s capsule
Contains specialized cells called podocytes or visceral epithelial
cells extending processes around the glomerular capillaries

The foot processes interdigitate with foot processes of


neighboring podocytes, a feature that can be clearly seen with
the scanning electron microscope

Elongated spaces between the interdigitating foot processes,


called filtration slits, are about 40 nm wide and covered by an
ultrathin filtration slit diaphragm
Histology of Renal Corpuscle
Filltration slit diaphragm revealed its complex protein
structure as a zipper-like sheet configuration with a
central density

A transmembrane protein, nephrin is a key structural and


functional component of the slit diaphragm

Nephrin molecules emerging from opposite foot processes


interact in the center of the slit (homophilic interactions),
forming a central density with pores on both sides
Glomerular basement membrane (GBM)

A thick (300 to 370 nm) basal lamina that is the joint


product of the endothelium and the podocytes

It is composed of a network consisting of type IV


collagen, laminin, nidogen, and entactin, together with
heparin sulfate proteoglycans such as agrin and
perlecan, as well as multiadhesive glycoproteins
Glomerular filtration barrier

Fenestrated Capillary Endothelium

Filtration membrane or GBM

Filtration slit diaphragms located between


the podocyte pedicels
Glomerular filtration barrier
Glomerular filtration
barrier

The fenestrations of the capillary


endothelium, which blocks blood
cells and platelets

The thick, combined basal laminae,


or GBM, which restricts large
proteins and some organic anions
The filtration slit diaphragms
between pedicels, which restrict
some small proteins and organic
anions.
Parietal layer of Bowman’s capsule

Contains parietal epithelial cells and forms a simple squamous


epithelium
At the urinary pole of the renal corpuscle, the parietal layer is
continuous with the cuboidal epithelium of the proximal convoluted
tubule
The space between the visceral and parietal layers of Bowman’s
capsule is called the urinary space or Bowman’s space

At the urinary pole of the renal corpuscle, the urinary space is


continuous with the lumen of the proximal convoluted tubule.
Mesangium

In the renal corpuscle, the GBM is shared among several capillaries to


create a space containing an additional group of cells called mesangial
cells
Mesangial cells are enclosed by the GBM, cells and their extracellular
matrix constitute the mesangium

Mesangium is most obvious at the vascular stalk of the glomerulus

Some are located outside the corpuscle along the vascular pole, where
they are also designated as lacis cells
Mesangial cells
• Physical support of capillaries
• Adjusted contractions in
response to blood pressure
changes
• Phagocytosis of protein
aggregates adhering to the
glomerular filter
• Immune defense and repair in
the glomerulus
Nephrotic syndrome

Mutations in the nephrin gene (NPHS1) are


associated with congenital nephrotic
syndrome, a disease characterized by
massive proteinuria and edema
Functions of the Mesangial Cells

 Phagocytosis and endocytosis


 Structural support
 Secretion
 Modulation of glomerular distension
Mesangial cells proliferation

Mesangial cells proliferate in certain kidney diseases in


which abnormal amounts of protein and protein complexes
are trapped in the GBM.

Proliferation of mesangial cells is a prominent feature in the


immunoglobulin A (IgA) nephropathy (Berger
disease),membranoproliferatie glomerulonephritis, lupus
nephritis, and diabetic nephropathy
Proximal Convoluted
Tubule
Simple cuboidal epithelium

Central nucleus

Microvilli

Long abundant mitochondria

Basolateral infoldings
Proximal Convoluted Tubule
Proximal Convoluted
Tubule

Specialized for both reabsorption


and secretion

Water and certain solutes passive


resorption

Small proteins receptor-mediated


endocytosis

Organic anions and cations secretion


Proximal Convoluted
Tubule

Hydroxylation of
vitamin D

Production of
etrythropoitin
Loop of Henle

Thin descending limb


and a thin ascending
limb

Simple squamous
epithelia
Loop of Henle

Thin descending
limb and a thin
ascending limb

Simple
squamous
epithelia
Loop of Henle

The straight part of the proximal tubule has an outer diameter of about 60 μm,
but it narrows abruptly to about 30 μm in the thin limbs of the loop.

The wall of the thin segments consists only of squamous cells with few
organelles (indicating a primarily passive role in transport) and the lumen is
prominent
The thin ascending limb of the loop becomes the thick ascending limb
(TAL), with simple cuboidal epithelium and many mitochondria again, in the
outer medulla and extends as far as the macula densa near the nephron’s
glomerulus.
The loops of Henle and surrounding interstitial
connective tissue are involved in further adjusting
the salt content of the filtrate.

Cuboidal cells of the loops’ TALs actively transport


sodium and chloride ions out of the tubule against a
concentration gradient into the hyaluronate-rich
interstitium, making that compartment
hyperosmotic.

This causes water to be withdrawn passively from


the thin descending part of the loop, thus
concentrating the filtrate.
The thin ascending limbs reabsorb sodium chloride (NaCl)
but are impermeable to water.

The countercurrent flow of the filtrate (descending, then


immediately ascending) in the two parallel thin limbs
establishes a gradient of osmolarity in the interstitium of
the medullary pyramids, an effect that is “multiplied” at
deeper levels in the medulla.

Countercurrent blood flow in the descending and


ascending loops of the vasa recta helps maintain the
hyperosmotic interstitium. The interstitial osmolarity at the
pyramid tips is about four times that of the blood.

The countercurrent multiplier system established by


the nephron loop and vasa recta is an important aspect of
renal physiology in humans
Distal convoluted
tubule (DCT)

Simple cuboidal cells

Fewer mitochondria

No brush border

Na+ absorption regulated by


aldosterone from the adrenal
glands.
Proximal Convoluted Tubule Vs Distal
Convoluted Tubule (DCT)
Juxtaglomerular apparatus (JGA)

Macula densa

Juxtaglomerular
granular (JG) cells

Lacis cells
Juxtaglomerular apparatus (JGA)
distal tubule (D) and glomerulus (G). At that point
cells of the distal tubule become columnar as a
thickened region called the macula densa (MD).

Smooth muscle cells of the afferent arteriole’s (AA)


tunica media are converted from a contractile to a
secretory morphology as juxtaglomerular granule
cells (JG)

Lacis cells (L), which are extraglomerular mesangial


cells adjacent to the macula densa, the afferent
arteriole, and the efferent arteriole (EA).

In this specimen the lumens of proximal tubules (P)


appear filled and the urinary space (US) is
somewhat swollen
Collecting Ducts

Pale staining principal


cells
• Few organelles
• Sparse microvilli
• Primary cilium
• Rich in aquaporins

Intercalated cells
• Abundant mitochondria
• Maintain acid-base balance
Countercurrent Multiplier System

 It involves three structures:


 Loop of Henle
 Vasa recta
 Collecting duct
Proteinuria
Diabetic Glomerulosclerosis

Diabetic glomerulosclerosis, the thickening


and loss of function in the GBM produced as
part of the systemic microvascular sclerosis in
diabetes mellitus, is the leading cause of
(irreversible) end- stage kidney disease in
the United States.

Treatment requires either a kidney


transplant or regular artificial
hemodialysis.
Sickle Cell Nephropathy

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